Lung cancer is one of the frequently occurring cancers in the world that threatens the lives of the human population. About 1.2 million people contract lung cancer world-wide and about 25% of the cancer-related deaths are due to lung cancer. Also, the occurrence rate and the death rate are gradually increasing in Korea. According to a report of Korea Central Cancer Registry in 2008, there were 132,941 cancer incidences in average in Korea in the periods of 2003-2005, and 16,123 lung cancer incidences in annual average for male and female indicating that 12.1% of total cancers are lung cancer placing second most commonly occurring cancer in Korea (Ministry of Health & Welfare, Korea Central Cancer Registry, Oct. 15, 2008).
It is known that a 5-year survival rate of lung cancer exceeds 80% if the lung cancer was found early in IA stage (Mulshine, J. L. and Sullivan, D. C. Clinical practice. Lung cancer screening. N. Engl. J. Med. 2005; 352:2714-2720). It is therefore important to find good markers that enables early discovery of lung cancer in pursuit of specific biological markers. Especially, lung cancer is a representative heterogeneous tumor, and the response and the prognosis are different for a variety of treatments. Lung cancer can be divided into two major categories medically, small cell lung cancer and non-small cell lung cancers (NSCLC). Non-small cell lung cancers can be further divided into lung adenocarcinoma, squamous cell carcinoma and large cell carcinoma.
Meanwhile, CD66c is known as CEACAM6 (Carcinoembryonic antigen-related cell adhesion molecule 6) or NCA (non-specific cross-reacting glycoprotein antigen)-90 and has a higher concentration in the blood of lung cancer, pancreatic cancer, breast cancer, rectal cancer and hepatoma patients. The above CD66c is an important protein for cell adhesion and is involved in adhesion of endothelial cells activated by cytokine in case of neutrophils.
Also, normal cells destroy themselves if cell adhesion is prevented. This process is called anoikis. Tumor cells, however, are resistant to such anoikis and promote cancer outbreak and metastasis of cancer as a result. There is a report that the above CD66c prevents anoikis, and there also is a report that malignant phenotype changes in cancer cells by regulating the expression of CD66c. Also, when the protein expression is inhibited by silencing CD66c genes by using small interfering RNA, metastasis is inhibited by enhancement of anoikis in vivo. In conclusion, metastasis can be prevented by inhibiting the function of CD66c.